It has traditionally been believed that aging occurs after the human body experiences an accumulation of damage. For instance, the molecular damage that oxidative stress causes to cells.
But, a new study conducted by scientists from the University of Birmingham has suggested that aging is instead the product of design flaws in our DNA code. In other words, the software that manages the development of single cells into adult organisms.
The researchers pondered how aging could happen so uniformly in spite of current models, which depend on the assumption that humans randomly accumulate “damage.”
Think of human development as the result of a computer program that is encoded in DNA. Using this analogy, the team suggested that aging is not the result of hardware damage accumulation but instead a process that is fueled by flaws in our DNA “software.”
“Our model is controversial as it challenges the prevailing view of aging as a result of random damage to the body’s hardware,” explained João Pedro Magalhães, who led the study.
“Instead, we suggest that aging is an information problem that is driven by design flaws in our body’s software. As the developmental program runs early in life, it is beneficial, but its runs later in life become detrimental and drive tissue degeneration and aging phenotypes.”
While radically different from past damage-based theories, the model of aging proposed by the team is reflected by fluctuating cellular information states that shift throughout the course of our lives.
This idea that aging is the result of our developmental software program helps to explain why some species which are closely related to humans still age at drastically different rates. Additionally, it illuminates the major pharmacological, dietary, and genetic manipulations of animal aging.
The suggestion that aging is an information problem, as opposed to damage-caused, could have significant implications for intervention developments to slow or even reverse aging processes.
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